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Diminished LcrV secretion attenuates Yersinia pseudotuberculosis virulence.
Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi.
Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet). Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). (Francis)ORCID-id: 0000-0001-6817-9535
Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet). (Forsberg)
2007 (engelsk)Inngår i: J Bacteriol, ISSN 0021-9193Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Many Gram negative bacterial pathogenicity factors that function beyond the outer membrane are secreted via a contact-dependent type III secretion system. Two types of substrates are predestined for this mode of secretion; anti-host effectors that are translocated directly into target cells and the translocators required for targeting of the effectors across the host cell membrane. N-terminal secretion signals are important for recognition of the protein cargo by the type III secretion machinery. Even though such signals are known for several effectors, a consensus signal sequence is not obvious. One of the tranclocators, LcrV, has been attributed other functions in addition to its role in translocation. These functions include regulation, presumably via interaction with LcrG inside the bacteria and immunomodulation via interaction with TLR2. Here we wanted to address the significance of the specific targeting of LcrV to the exterior for its function in regulation, effector targeting and virulence. The results, highlighting key N-terminal amino acids important for LcrV secretion, allowed us to dissect the role of LcrV in regulation from that in effector targeting/virulence. While only low levels of exported LcrV were required for in vitro effector translocation as deduced by a cell infection assay, fully functional export of LcrV was found to be a prerequisite for its role in virulence in the systemic murine infection model.

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2007.
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URN: urn:nbn:se:umu:diva-16663PubMedID: 17873031OAI: oai:DiVA.org:umu-16663DiVA, id: diva2:156336
Tilgjengelig fra: 2007-10-08 Laget: 2007-10-08 Sist oppdatert: 2018-06-09

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